Antenatal Testing Modalities

Modalities of Antepartum Fetal Testing

Extra Reading:

  • ACOG PB 229 (Antepartum Fetal Surveillance)

  • CO 828 (Indications for Antepartum Fetal Surveillance)

What we won’t do:

  • Talk about frequency / timing / specific indications for testing 

    • CO 828 provides a great overview of this as a reference, and we’ll obviously mention our own practice for testing in subject-specific episodes!

    • Various institutions may have their own policies and procedures that you should be aware of.

Rationale / Techniques of Antenatal Testing

  • Testing techniques are meant to detect changes in fetal status, particularly in response to hypoxemia and acidemia.

    • Hypoxemia and resulting metabolic acidemia redirect fetal blood flow; for instance, decreasing renal perfusion and resulting on oligohydramnios.

      • Other physiologic changes such as decreased heart rate variability and decreased fetal movement or poor muscle tone can be appreciated. 

    • Progressive metabolic acidosis In these situations can result in stillbirth / fetal death – the primary outcome we are looking to avoid by employing this testing.

      • Antepartum surveillance is generally indicated for any condition which raises the risk of stillbirth.

        • In CO 828, the “cutoff” for included indications is defined as 0.8 / 1000 deliveries for a given condition, which is about twice the odds of stillbirth at term in otherwise low risk pregnancies

        • This is also the false-negative rate of a BPP, providing further justification for this cutoff.

    • Importantly, any fetus with neurologic depression/anomalies may still be at increased risk for stillbirth, but antenatal testing may not be as equipped to detect risk.

    • Similiarly, the utility and predictive value are less at earlier gestational ages.

Maternal kick counts

  • A complaint of decreased in fetal movement has been demonstrated as a risk for stillbirth, which is why we ask folks to come to be assessed for it! 

  • How effective are routine kick counts?

    • A meta-analysis of five RCTs and over 450,000 fetuses found no differences in stillbirth rate between groups undergoing routine kick counts, and those who did not. 

      • However, stillbirth rate in the trials overall was low – 0.54% in the kick count group, and 0.59% in the control group, with the confidence interval for the relative risk ranging from 0.85 – 1.00 – so while crossing 1 and thus being statistically non-significant, may lay more towards benefit with additional study.

        • Those in the kick count group did experience slightly higher rates of preterm delivery, labor induction, and cesarean delivery – perhaps some harm from this?

        • Likely, more studies are necessary to help make better determinations regarding the utility of kick counts.

  • How should we tell people to do kick counts?

    • The practice bulletin mentions one trial instructing patients to lie on their side and count 10 movements over a 2 hour period as reassuring – we trained with this as the recommended way!

      • The bulletin also mentions another to count movements for 1 hour three times per week, and reassuring was considered to be if the movement number “equals or exceeds the previously established baseline count” – seems a bit more complicated! 

  • There definitely isn’t robust evidence to do routine fetal movement assessments, or to use that as a testing technique – but again, definitely have your patients present to care for any sense of decreased movement!

Non-Stress Test (NST)

  • The NST is the classic method for antenatal testing. It’s based on the notion that if the fetus is not acidotic, the heart rate variability will be appropriate, and the heart rate will accelerate with fetal movement. 

  • The heart rate should be monitored for at least 20 minutes, but may require longer periods due to fetal sleep cycles.

    • Vibroacoustic stimulation (VAS) is permissible to obtain a stimulated acceleration – it won’t falsely reassure you abut acid-base status, and can decrease the amount of time you’re waiting through a sleep cycle! 

      • Per the PB, stimulus should be applied for 1-3 seconds and may be repeated up to three times for a valid NST.

  • Test results are conveyed as reactive or non-reactive

    • Even though this is the same tech as continuous monitoring in labor, we don’t use the same terminology! So don’t call an NST “category 1” – the only results are reactive or non-reactive. 

      • Reactive means that there should be two or more accelerations in a 20-minute period. 

        • Accelerations should be 10 beats elevation over 10 seconds (10x10) at less than 32 weeks, and 15 x 15 at greater than 32 weeks.

      • Non-reactive means that over 40 minutes of monitoring, the acceleration criteria is not met.

      • So can you have decels in a “reactive” NST? – yes! Remember – “category” system in labor is different than NST description!

        • Variable decelerations that are non-repetitive and brief (< 30 sec) are not associated with fetal compromise or need for obstetric intervention. 

          • If repetitive (>3 in 20 mins), there is increased risk for cesarean delivery for non-reassuring monitoring, and so should be considered for additional testing.

        • Decelerations lasting for over 1 minute during an NST is associated with a high risk of cesarean as well as stillbirth – so additional testing or delivery should be considered if present.

    • One common question – when should an NST be reactive?

      • This is hard to answer – studies have looked at this using the original 15x15 criteria:

        • At 24-28 weeks, up to 50% of NSTs are non-reactive

        • At 28-32 weeks, up to 15% of NSTs are non-reactive

      • For this reason, the 10 x 10 criteria was proposed and deemed sufficient, but certainly the rate of non-reactive tracings are much higher at earlier gestational ages, and so some institutions adjust monitoring protocols accordingly prior to 28-32 weeks.

Contraction Stress Test (CST)

  • A step-up from the NST – now, we look to interpret the fetal heart rate response to provoked uterine contractions.

    • Since contractions cause some transient fetal deoxygenation, a fetus that is compromised already will demonstrate inability to compensate physiologically – and thus show decelerations.

  • There’s a lot of vocabulary regarding the CST, so let’s start with how the test is run:

    • An adequate CST requires three contractions persisting for at least 40 seconds each in a 10 minute period. If the CST is inadequate, contractions can be stimulated with IV oxytocin or nipple stimulation.  

      • In this testing, nipple stimulation actually is very useful, and can achieve adequate testing in half the time required versus IV oxytocin!

  • Once the test is adequate, it should be monitored similarly to an NST over 20 minutes. The test results can be one of five options:

    • Negative: No late or significant variable decelerations elicited. A “negative” CST means the fetus is not compromised.

    • Positive: late decelerations are present after 50% or more of contractions. This is also a possible interpretation even with an inadequate CST. Thus, a “positive CST” suggests compromise of the fetus.

    • Equivocal-suspicious: Intermittent late decelerations or significant variable decelerations are present. 

    • Equivocal: FHR decelerations in the presence of contractions that are occurring more frequently than every 2 minutes, or lasting longer than 90 seconds. This suggests that tachysystole or contraction strength may be compromising the validity of the test.

    • Unsatisfactory: synonymous with an inadequate CST – that is, fewer than three contractions in 10 minutes; alternatively, if the tracing is uninterpretable. 

  • CSTs are great and often overlooked tools but should not be performed, generally speaking, in conditions that are contraindications to labor or vaginal delivery – i.e., placenta previa.

Biophysical Profile (BPP) and Modified BPP

  • The BPP combines an NST with up to four ultrasound criteria, which are:

    • Amniotic fluid volume: per the practice bulletin, a single deepest vertical pocket of greater than 2 cm is adequate.

      • Some practices may use the amniotic fluid index instead, or in addition to, a measurement of the deepest vertical pocket. RCTs suggest that DVP is acceptable and may even be preferred. 

    • Fetal movement: three or more discrete body or limb movements. 

    • Fetal tone: one or more episodes of extension of a fetal extremity with return to flexion, or opening and closing of a hand.

    • Fetal breathing movements: One or more episodes of fetal breathing movements of 30 seconds or more. 

      • All of the ultrasound criteria should be observed in 30 minutes or less. 

      • Each component is scored as a 0 (if criteria not met) or 2 (if criteria met), including the NST. 

        • 8-10 / 10: normal

        • 6 / 10: equivocal - generally repeat in 6-12 hours

        • 4 or less / 10: abnormal -- context dependent - deliver or repeat testing pending situation

  • The modified BPP consists of just the NST in addition to assessment of amniotic fluid volume. If either of these is abnormal, the usual next step is to proceed with the remainder of the BPP. 

    • Oligohydramnios is a separate and significant risk for stillbirth – remember that delivery is recommended for this starting at 36’0 or later! Additional testing should definitely be performed if this is seen earlier than 36 weeks. 

    • If you’re seeing lots of decels – then resuscitate/deliver!

      • A BPP can’t reassure you about decels, which suggest some sort of acute decompensatory event is occurring.

Umbilical Artery Doppler Velocimetry (UAD)

  • UAD is a special ultrasound technique that is generally most useful in monitoring fetuses affected by growth restriction.

    • The umbilical artery blood flow in cardiac diastole is very high in normally-growing fetuses.

    • In the growth restricted fetus, blood flow in diastole may be reduced, absent, or reversed; and with these abnormalities, perinatal mortality and stillbirth risk are significantly increased. 

      • This is particularly true in the presence of absent or reversed end-diastolic flow. 

  • There is no evidence at present that UAD helps to provide more information about fetal well-being in other situations; so FGR is the only place you’ll routinely see it employed in obstetrics. 

  • Listen to our FGR podcast to learn more! 

What is the comparative predictive value/efficacy of these tests?

  • The evidence for antenatal testing is largely circumstantial; that is, stillbirth risk seems reduced compared to unmonitored pregnancies, which are largely historic cohorts before current technology was available.

  • We can state with confidence that testing has high negative predictive value.

    • Normal test results in most cases are highly reassuring, as these tests are associated with low false-negative rates – with a false negative defined as a stillbirth within 1 week of the normal result. Fer each modality:

      • NST: 1.9 per 1,000; aka, negative predictive value of 99.8%

      • CST: 0.3 per 1,000: aka, NPV of >99.9%

      • BPP: 0.8 per 1,000: aka, NPV of >99.9%

      • Modified BPP: 0.8 per 1,000: aka, NPV of >99.9%

      • UAD: less studied, but best available evidence suggests an NPV approaching 100% as well. 

  • Again, these tests can help reduce risk of stillbirth with chronic conditions; acute conditions, such as abruption or cord accident, cannot be predicted with these modalities.  

Oxygen: Friend or Foe?

Shout out to Chelsea Jorgenson, nurse at UW Medical Center, for the episode idea! 

Oxygen is a drug.

The FDA regulates medical gases like oxygen as a drug, with the approved indications of hypoxia and hypoxemia. Did you know these are different?

  • Hypoxemia: reduced partial pressure of O2 in the blood (low PaO2).

  • Hypoxia: reduced tissue levels of O2 so that cellular metabolism is impaired.

    • Hypoxemia generally precedes hypoxia. 

      • You have less oxygen to deliver, so there’s less O2 in the tissues over time. 

    • Hypoxemia does not always result in hypoxia

      • For instance, those who live at high altitude can by hypoxemic, but not hypoxic. 

Like other drugs, oxygen has benefits, but also has potential harms. And for a quick review of the benefits/harms of oxygen medically, check out the Journal of Hospital Medicine’s series, “Things We Do For No Reason.”

Many studies have shown, mostly on animal models, that hyperoxygenation leads to lung injury, inflammation through free radical generation, and changes in perfusion that may actually be harmful:

    • COPD: oxygen titrated to goal >88-92% is associated with 2x fold increased mortality risk.

      • Linked likely due to worsened ventilation-perfusion matching and poorer CO2 offloading as PaO2 rises (Haldane effect). 

    • MI: 1976 RCT of O2 in suspected MI patients at 6L/min. Patients receiving for 24 hours or more had more episodes of tachycardia with no improvement in mortality, analgesic use, or infarct size. 

      • Subsequent trials have found similar outcomes, and actually have also demonstrated increased rate of MI recurrence with O2 use.

      • European Society of Cardiology has now actually recommended no O2 use unless SpO2 < 90% for MI patients! 

    • Retinopathy of prematurity: hyper oxygenation of neonates increases risk of blindness.

    • Other illness: trials in settings ranging from ICUs, strokes, TBIs, and cardiac arrest have also linked liberal O2 use (ranging from 2L NC upwards) to increased mortality and other adverse events.

      • A meta analysis demonstrated a dose-dependent toxicity: for every 1% increase of SpO2 above 94-96%, there was 25% relative increase in in hospital mortality!!! 

So when is oxygen helpful?

Importantly, these studies have mostly looked at normoxemic patients who receive supplemental oxygen. Patients who are significantly hypoxemic or hypoxic will certainly benefit from O2. 

Additionally, patients with conditions such as CO poisoning, cluster headaches, sickle cell crisis, and pneumothorax may all benefit from O2. These are actual indications for the drug.

OK, so what about pregnancy and labor?

O2 is most commonly administered in labor, in an attempt to improve fetal status. The thought being that, if we see significant decelerations that reflect fetal hypoxia, administration of supplemental oxygen through the mother/placenta will help to correct it. 

  • Pro oxygen evidence:

    • Fetal pulse oximetry studies 2 small studies using a fetal pulse-oximeter in laboring women demonstrated increased fetal oxygenation of 5% with simple face masks, and 7-15% when using non-rebreathers, in non-hypoxic fetuses. In hypoxic fetuses, the observed benefit was greater, 20% with simple face mask and 26-37% with non-rebreather. 

      • Fetal pulse oximetry did not help to improve rates of cesarean delivery for fetal indications, and thus has not caught on as a routine technology in labor management. Thus critics would argue it’s hard to interpret these studies in context of whether O2 improves neonatal outcomes, or just makes the saturation numbers better.

  • Anti-oxygen evidence:

    •  Fetal scalp pH study:a small study examining the effect of administering 50-10% oxygen during first stage of labor actually had no effect on fetal scalp pH, and trended towards a worsening base deficit with supplemental O2. Another study of primates administered O2 with acidotic fetuses by scalp pH demonstrated worsening of acidosis with O2 administration. 

      • These studies though, like the others, were small and nonrandomized. There is also criticism in the timing and application of O2 in each of these trials. 

    • Non-inferiority RCT: a 2018 RCT in JAMA used a non-inferiority approach to randomize 114 patients to supplemental O2 versus room air with category II EFM. They found no difference between groups in improving umbilical artery lactate, which was their primary marker for this trial.

      • There was also no difference in other cord gas components or rates of cesarean delivery for fetal indications. 

      • Umbilical artery lactate does have some ability to predict hypoxia-associated morbidity in neonates; however, it is not sensitive or specific for poor outcomes, a valid criticism. The trial was not powered for neonatal outcomes. 

    • A secondary analysis of this same RCT looked at umbilical venous O2 concentration and actually found lower O2 pressure in fetuses exposed to long periods of O2 than those exposed for short periods or on room air. 

The physiologic arguments for (or against) O2

Check out our fetal circulation episode for a quick review of how blood and oxygen travel in the fetus!

The maximum fetal PO2 (i.e., in the umbilical vein at the site of the placenta) cannot exceed maternal venous PO2. This is why fetal hemoglobin has to have a very high oxygen affinity, as it must extract O2 away from the venous side of maternal blood, which already is at a lower oxygen concentration. 

An oxygen dissociation curve. Fetal hemoglobin maintains relatively excellent saturations, even at usual venous O2 pressures in maternal circulation (HbA). Source: WIKIPEDIA.

  • A normal venous Po2 in adults is around 35-45 mmHg (arterial is around 100 mmHg). That would equate on a HbA dissociation curve to a saturation of around 65-75%. 

  • A normal Po2 in a venous cord gas, by comparison, is on average around 35mmHg, again representing maternal venous O2 tension. 

    • But the fetal hemoglobin affinity for O2 powers this to about an 80-90% saturation! And that is considered normal -- most O2 saturation values at the 5 minute Apgar are in the mid-80%s.

  • The question lies herein: by causing maternal hyperoxemia, will that result in fetal recovery if the fetus is hypoxic? 

    • By increasing the PaO2 in the mother with supplemental oxygen, theoretically there would be an increased oxygen gradient to diffuse downstream to the fetus. 

      • In effect, because there is more oxygen tension, the higher the maternal PvO2 and umbilical vein O2 pressure can become.

    • But as we discussed with ischemic events, sometimes oxygen may counterintuitively not improve outcomes, or mask worsening of the process! 

      • In this case, the fetus becomes hypoxic, or the “ischemic” tissue -- would the new O2 load in this case be detrimental? 

      • Or potentially, like in COPD, would the normoxemia actually mask worsening acidosis? 

      • Or finally, as demonstrated in the RCT we referenced, does the O2 even get to the fetus due to some placental transfer failure in the presence of hyperoxia?

What should the bottom line takeaway be?

That’s the other interesting thing about this -- in spite of the fact that there is little evidence supporting this practice, O2 is wildly popular as a resuscitative effort. It’s simple and quick to apply. 

Intrauterine resuscitation, defined as repositioning, oxytocin discontinuation, fluid administration, amnioinfusion, or oxygen administration in response to fetal heart rate tracing abnormalities, are all options. 

While we couldn’t identify any studies that shared the “natural history” of what’s done during a deceleration, anecdotally we know that reflexively, reaching for the facemask oftentimes will precede these other measures, despite the evidence on decelerations favoring these other options. In short, leave O2 for maternal hypoxia, or as a last-resort option for fetal resuscitation! 

Cardiotocography/EFM Part II: Management

Today we are back with our midwifery colleagues Linda Steinhardt and Liz Kettyle, who shepherd us through the management of cardiotocography in labor.

We start this episode by quickly reviewing definitions, and defining categories of tracings, reviewed below:

Copyright UpToDate

Recall that category I tracings virtually exclude fetal acidemia, while category III tracings are associated with acidemia 25% of the time, but also have higher risk of cerebral palsy, neurologic injury, or fetal death. That said, the positive predictive value for bad outcomes of CTG is overall poor.

We review a number of scenarios and resuscitative measures for category II and III tracings. However, much of this episode draws on the 2013 Clark et al. article to describe the management of category II tracings. The algorithm is below:

Clark et al. (AJOG 2013)

Interpreting Cardiotocography/EFM Part I: Definitions

Today we take a break from STIs to jump back into obstetrics, and are joined by two very special guests: Liz Kettyle and Linda Steinhardt, both of whom are certified nurse midwives (CNMs) and clinical educators at the Warren Alpert Brown School of Medicine.

ACOG PB 106 (membership required) forms the basis for this episode and in a future episode, we will discuss management of cardiotocography (CTG). Also, for a recent article surrounding the naming of CTG vs. EFM vs. all the other names for this technology, check out a recent AJOG article on its now 50-year history.

We also are using some special sound effects for these episodes! As you listen to the various sounds for different types of decelerations, keep in mind that the higher-pitched sound represents a contraction pattern, and the lower-pitched sound represents the fetal heart rate response.